Support cells in the nervous system
POPULARITY
9 episodes with glial
4 episodes with glial
2 episodes with glial
14 episodes with glial
2 episodes with glial
2 episodes with glial
2 episodes with glial
2 episodes with glial
2 episodes with glial
In today's episode, we dive into the critical role of phospholipids in maintaining brain health, examining how these molecules contribute to neuronal communication, synaptic plasticity, and cognitive resilience. We'll explore the biochemical structure and function of key phospholipids like phosphatidylserine and phosphatidylcholine within neuronal membranes, where they play indispensable roles. We discuss associations and impacts of environmental toxins, aging, and neurodegenerative conditions. Finally, we discuss dietary tools to support phospholipid levels and promote cognitive health. Topics: 1. Introduction to Phospholipids and Cognitive Health 2. Brain Cell Structure and Composition - Neurons, glial cells. 3. Detailed Anatomy of Neurons - Soma contains organelles, dendrites receive signals, axon sends impulses. - Myelin sheath insulates axon, speeding signal transmission. - Myelin is rich in phospholipids. 4. Roles of Glial Cells in Brain Health - Astrocytes, oligodendrocytes, and microglia support neurons. - Glial cells regulate the brain's environment, form myelin, and provide immune defense. - Phospholipid-rich membranes are essential for glial function. 5. Biochemistry: Phospholipids - Phospholipids have a glycerol backbone, fatty acid tails, and a phosphate group. - Hydrophilic and hydrophobic parts form bilayers. - Key phospholipids: PC, PE, PS, PI 6. Phospholipid Bilayer's Role in Neuronal Communication - Ion channels, receptors, and transporters in the bilayer enable cell functions. - Ion channels allow ions to flow, creating signals for neuron communication. - Receptors detect neurotransmitters, initiating responses. 7. Neuronal Activation and Electrochemical Gradients - Resting neurons have ion concentration differences inside and outside the cell. - Ion channel activity during activation creates an action potential. - The phospholipid membrane enables controlled ion flow for signal transmission. 8. Neurotransmitter Release - Action potential at axon terminal triggers calcium entry. - Calcium causes vesicles to release neurotransmitters. - Released neurotransmitters bind to receptors, continuing the signal. 9. Diversity of Phospholipids in Neuronal Membranes - Different phospholipids (PC, PE, PS, PI) are essential for membrane integrity. 10. Summary: Phospholipids in Brain Function and Cognitive Health - Phospholipids support neuronal communication, synaptic plasticity, and cognitive resilience. - Synaptic plasticity - essential for learning and memory. 11. Phospholipid Disruption and Cognitive Decline - Oxidative stress, aging, and inflammation disrupt phospholipid composition. - Lipid peroxidation damages membranes, affecting neuron signaling. - Phospholipid damage contributes to cognitive decline. 12. Importance of Phospholipids in Aging and Brain Health - Lipid levels decrease with age, impacting brain function. 13. Environmental Toxins and the Brain - Heavy metals like mercury cause oxidative damage to phospholipids. - Damaged phospholipids and impaired neuron function. 14. Consequences of Suboptimal Phospholipids - Cognitive symptoms. - Low levels seen in neurodegenerative conditions. 15. Tools for Supporting Phospholipid Levels - Foods with PS and PC, such as fatty fish and eggs. - Phospholipid supplements. Thanks for tuning in! "75 Gut-Healing Strategies & Biohacks" Follow Chloe on Instagram @synthesisofwellness Follow Chloe on TikTok @chloe_c_porter Visit synthesisofwellness.com --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support
Join me for a summary looking into the increasingly popular topic of paediatric obstructive sleep apnoea, a review of orthodontic treatments available, and how effective they are in this growing field of both medicine and dentistry. This episode is a summary of Alberto Capriglio's lecture from the AAO and Carlos Flores Mir's lecture at the IOF earlier this year. OSA - Defined upper airway dysfunction causing complete or partial airway obstruction during sleep Sleep = Slow wave sleep – constructive phase of sleep (recuperation of the mind) · Growth hormones secreted · Glial cells within brain restored · Cortical synapses increase in number – Moberget 2019 Outcomes to paediatric patients of SDB: (AASM) · delays in development, Poor academic performance, Aggressive behaviour, attention- deficit/hyperactivity disorder, , emotional problems in adolescence First line medical treatment – adenotonsillectomy · 40% residual OSA Effect palatal expansion 1. Roof the mouth = base of the nose - Increase in nasal airway volume - Reduction in OSA, if obstruction in naso-pharynx, 2. Short term reduction in OSA (not cure AASM) a. 20% improvement in AHI, 85% of cases Villa 2015 b. 15% got worse by 20% c. 57.5% residual AHI greater than 1 - not resolution 3. Caprioglio 2019 long term AHI return to initial scores, from 7 to 5 long term 4. Change in metabolism when combined with Vit D3 a. Vit D3 with RME increases reduction in AHI, sustained long term, Caprioglio 2019 AHI 61.9% Vs 35.5% long term Expansion other outcomes - school performance Bariani 2024 · AJODO – RME improves academic performance – o BEHAVOUR 1 of 8 parameters improved only for academic performance - change small 0.68 o COGNITIVE 1 in 8 improve Mandibular advancement Move mandible forwards and open space behind the tongue – oropharynx · Anatomical – increase size of oropharangeal airway · YAnyAn 2019 mandibular advancement for pOSA systematic review: 1.75 AHI reduction (CI) −2.07, −1.44) – modest change · However long term use required of the paediatric patient Orofacial features in children with obstructive sleep apnea. Fagundes Flores-Mir 2022 o No craniofacial features specific to pOSA – ANB, o However medical diagnosis through polysomnography may under-estimate incidence, o Broader diagnosis such as snoring, may over-estimate OSA AADSM 2024 – consensus statement · Expansion o Prevention: No consensus o Management: No consensus o Cure: Insufficient · Mandibular advancement o Prevention, management, cure – unclear More about OSA? To hear more about OSA, please check out the last interview on orthodontics in interview with Sanjivan Kandasamy, where we had a deep dive into OSA and where we are in our understanding today from the research Interview with Sanjivan Kandasamy on OSA
Half of the cells in the brain are neurons, the other half are glial cells.When scientists first discovered glia over a century ago, they thought that they simply held the neurons together. Their name derives from a Greek word that means glue.In the past decade, researchers have come to understand that glial cells do so much more: They communicate with neurons and work closely with the immune system and might be critical in how we experience pain. They even play an important role in regulating the digestive tract.Ira is joined by Yasemin Saplakoglu, a staff writer at Quanta Magazine who has reported on these lesser-known cells.Transcripts for each segment will be available after the show airs on sciencefriday.com. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.
In this episode, Dr. Kharrazian delves into the world of hormone imbalances, microbiome diversity, and the impact of polyphenols and phytoestrogens. He discusses evidence-based strategies for autoimmune disease, brain health issues, and chronic health conditions, and sheds light on the pivotal role of gut health in estrogen metabolism. He also addresses nutraceutical support for insulin resistance and regulating testosterone. For patient-oriented courses, visit https://drknews.com/online-courses/For CE and CME practitioner courses, visit https://kharrazianinstitute.com/00:00 Transitioning off HRT may benefit from modulators.06:05 Flavonoids affect estrogen receptor, 4 key foods.10:05 Healthy microbiome diversity enhances effectiveness of soy products.11:16 Carbs impact conversion of phytoestrogens efficiently.16:29 Gut health crucial for managing estrogen disorders.18:57 Diet, lifestyle, supplements affect microbiome diversity.20:53 Liver pathways detoxifying hormones, potential competition. Nutrients aid hepatic inflammation support.26:51 Essential fatty acids are critical for health.30:29 Prostate glands cause pelvic issues, need support.34:19 Men's testosterone, estrogen testing, insulin resistance, obesity, blood sugar imbalances, hypoglycemia, insulin resistance, dietary guidelines.36:02 Optimize diet to prevent blood sugar crashes.39:41 Review found herbal medicines improve PCOS symptoms.42:41 Aggressive protocol for PCOS using nutraceuticals.47:19 Nutraceuticals may protect serotonin cells, boost testosterone.50:44 Botanicals boost testosterone levels but may vary.53:42 Glial cells switch to pro-inflammatory state. Hormone changes amplify neuroinflammation.56:35 Peptides stimulate hormones, potential for endocrine treatment.58:37 Dr. Kharrazian's podcast and blog information.Support this show http://supporter.acast.com/solving-the-puzzle-with-dr-datis-kharrazian. Hosted on Acast. See acast.com/privacy for more information.
In this episode, we take a deep dive into the intricate world of hormone imbalances and hormone replacement therapy. Dr. Kharrazian discusses the latest research findings, revealing a clear linear dose-response relationship between oral contraceptive use and the risk of hypertension, as well as the links between hormone replacement therapy and various health concerns. We explore the complexities of hormone disorders and the need for a personalized approach to treatment, discussing the impact of hormones on clinical function, the liver, and the gut microbiome. Join us as we uncover the vital connection between hormones and overall health, as well as the challenges individuals face in receiving appropriate evaluation and treatment for hormone-related issues in the current healthcare system.Learn more at drknews.com00:00 Hormone disorders treated with diverse approaches.08:13 Hormone replacement therapies and over-the-counter options.14:10 Different types of hormonal contraceptives can cause weight gain and mood disorders.18:50 Glial cells produce main hormone for synaptic activity.25:45 Hormone replacement therapy not recommended for everyone.30:43 Testosterone therapy shows health benefits with low risk.37:49 Variety of lifestyle strategies for hormone balance.39:54 Viral infection may require immediate symptom management.48:43 Stimulating dysfunctional gland, hormones, pituitary issues, hormones.53:18 Protein pathways impact hormone levels causing symptoms.58:19 Androgel may not effectively metabolize into hormones.01:02:16 Microbiome dysbiosis consequences, particularly linked to hormones.01:08:23 Estradiol strongest, estrone not as strong.01:11:19 Urinary labs may not accurately test hormones.01:16:20 Maintain resiliency for hormone levels, health longevity.Support this show http://supporter.acast.com/solving-the-puzzle-with-dr-datis-kharrazian. Hosted on Acast. See acast.com/privacy for more information.
Episode Notes:Andrew's happiest memory. What signs or symptoms should parents be vigilant about to detect potential serious health issues in their child?How does maintaining motivation play a significant role in the overall battle against cancer?What kind of support systems are crucial for parents who are taking care of a child with a serious illness?And much more! About Andrew Miller:A courageous, highly spirited, and brave 9-year-old warrior battling two types of cancer…He was diagnosed with two types of Stage 4 cancer.1) High-grade glioma cancer (located in the right front lobe of his brain)...A glioma is a mass of cells or a tumor that forms when glial cells grow out of control. Glial cells support neurons, or nerves, in the central nervous system. A glioma that's considered “high-grade” spreads quickly. High-grade gliomas may not always be curable. They're challenging to treat because they grow rapidly into the brain or spinal cord.2) Adult B-cell lymphoma cancerThat refers to a group of cancers that affect your immune system. It makes up 85% of all non-Hodgkin lymphomas, which are among the most common cancers in the United States. B-cell lymphoma frequently affects your lymphatic system, which is a network of lymph nodes, lymph vessels, and tissues that move fluid around your body.He now has so many little tumors starting in inoperable places.His ❤️Make-A-Wish❤️ is to receive 2,000 cards for Christmas and birthday, which just recently❤️If you would like to help out, mail card(s) to:BuddyTruman House Community Hospice716 Commercial Ave. SWNew Philadelphia, OH 44663He will soon be the author of an activity book of mazes (his favorite types).We will keep you updated on when and where you will be able to purchase his book and how you can support his mission... Connect with Barb!Host of #1 Rated The Kid Factor Podcast: https://podcasts.apple.com/us/podcast/the-kid-factor/id1707462012Linktree: https://thekidfactor.fun/linktreeWebsite: https://www.thekidfactor.fun/Facebook: https://www.facebook.com/TheKidFactor/ | https://www.facebook.com/groups/thekidfactorfamilyInstagram: https://www.instagram.com/thekidfactorofficial/LinkedIn: https://www.linkedin.com/in/barb-v-81497547/YouTube: https://www.youtube.com/channel/UCW9_PtybHaqXMrKFh8pId8wThank you so much for joining us today!If you enjoyed this episode, please submit a rating and review and share it with a friend. Together, we can inspire more people to utilize The Kid Factor!Let's keep the conversation going! We would love to hear from you and your wants, needs, and goals and support you along the way! Head over to our website at https://www.TheKidFactor.Fun, where we connect, collaborate, and celebrate each other while sharing more about money, business & entrepreneurship, and personal development. Can't wait to see you there!Make sure you pick up your FREE PDF TIPS FOR RAISING FINANCIALLY INDEPENDENT KIDS.DO YOU OR YOUR CHILD WANT TO WRITE AND PUBLISH YOUR OWN BOOK?Classes are forming NOW!Contact Barb today to learn about our publishing programs and scholarships!IF YOU OR SOMEONE YOU KNOW IS STRUGGLING WITH MENTAL HEALTH ISSUES... YOU"RE NOT ALONE>>>Website: https://www.nami.org/HomePhone: NAMI HELPLINE 800-950-6264 or TEXT "helpline" to 62640In 2020, the nation took a significant step forward with the enactment of the National Suicide Hotline Designation Act, a bill NAMI advocated for that created a nationwide three-digit number (988) to assist people experiencing a mental health or suicidal crisis. This number is now available in communities across the country.NAMI recognizes that other organizations have drawn distinctions between what diagnoses are considered “mental health conditions” as opposed to “mental illnesses.” We intentionally use the terms “mental health conditions” and “mental illness/es” interchangeably.A mental illness is a condition that affects a person's thinking, feelings, behavior, or mood. These conditions deeply impact day-to-day living and may also affect the ability to relate to others. If you have — or think you might have — a mental illness, the first thing you must know is that you are not alone. Mental health conditions are far more common than you think, mainly because people don't like to, or are scared to, talk about them. However:1 in 5 U.S. adults experience mental illness each year1 in 20 U.S. adults experience serious mental illness each year1 in 6 U.S. youth aged 6-17 experience a mental health disorder each year50% of all lifetime mental illness begins by age 14, and 75% by age 24A mental health condition isn't the result of one event. Research suggests multiple linking causes. Genetics, environment, and lifestyle influence whether someone develops a mental health condition. A stressful job or home life makes some people more susceptible, as do traumatic life events. Biochemical processes and circuits and basic brain structure may play a role, too.None of this means that you're broken or that you, or your family, did something “wrong.” Mental illness is no one's fault. And for many people, recovery — including meaningful roles in social life, school, and work — is possible, especially when you start treatment early and play a strong role in your own recovery process.THERE'S HELP & HOPE...
In the mid 1990's neuro scientists discovered that there was a lot more going on with Glial cells than they ever imagined. These cells appeared to be communicating, thinking amongst themselves. The late maverick artist and psychic Ingo Swann came to believed they were the centre of human telepathy. jay Katz and Aspasia hold a lively discussion with pharmacist Voytek Bereza about this and much more. Check him out on the link below.https://www.linkedin.com/company/the-transparent-company?trk=public_profile_topcard-current-companyThis show is part of the Spreaker Prime Network, if you are interested in advertising on this podcast, contact us at https://www.spreaker.com/show/4602609/advertisement
Join Jean Hebert, a leading expert in brain health, as he delves into the transformative potential of brain tissue replacement, brain computer interfaces, and their implications for reversing aging. In this comprehensive discussion, Jean shares insights on the science of brain restoration, the challenges and innovations in the field, and the broader implications of these technologies for the future of brain health and aging. Discover how modern science is pushing the boundaries of brain health and offering hope for a future where aging can be countered. TLDR: The key idea of the video is that brain tissue replacement has the potential to restore brain function and reverse aging, and industry partnerships could accelerate its development. Newsletter sign up (new and exciting developments) https://learningwithlowell.us12.list-manage.com/subscribe?u=08ed8a56013d8b3a3c01e27fc&id=6ecaa9189b Join this channel to get access to perks: https://www.youtube.com/channel/UCzri06unR-lMXbl6sqWP_-Q/join Over 321 books from 170 plus interviews over 5 years https://www.learningwithlowell.com/over-321-books-from-170-interviews-over-5-years-for-autodidacts/ https://youtu.be/MgqQq7DJSa4 PODCAST INFO: The Learning With Lowell show is a series for the everyday mammal. In this show we'll learn about leadership, science, and people building their change into the world. The goal is to dig deeply into people who most of us wouldn't normally ever get to hear. The Host of the show – Lowell Thompson- is a lifelong autodidact, serial problem solver, and founder of startups. LINKS Spotify: https://open.spotify.com/show/66eFLHQclKe5p3bMXsCTRH RSS: https://www.learningwithlowell.com/feed/podcast/ Youtube: https://www.youtube.com/channel/UCzri06unR-lMXbl6sqWP_-Q Youtube clips: https://www.youtube.com/channel/UC-B5x371AzTGgK-_q3U_KfA Website: https://www.learningwithlowell.com/ Jean Hebert links https://hebertlab.einsteinmedneuroscience.org/ https://hebertlab.einsteinmedneuroscience.org/about/ Timestamps / Chapters 00:00 Brain computer interfaces vs rejuvenation for brain damage 02:02 Why choose brain aging? 06:08 Specificity of tissue replacement 09:00 Rough timeline and what's left to develop 11:20 Jean Herbert's role at a spun out company 12:20 Startup transition / production compared to academia 14:00 Places to steal from 15:10 Amount needed to raise 16:20 Jean Hebert Thesis compared to Michael Levin to generate tissue 18:40 Neuro Cortical precursor cell types to include vs not include 21:10 Workhorse cells / Glial cells /precursor neurons 22:30 Prevent Scarring during tissue replacements 24:22 Suppressing immune system 27:05 Mice the best model for this research 30:00 AI in lab or expectations to use / FAN Q 33:13 Using surgical robots 34:00 Micro glial engineering project explained 36:40 Alzhemers / diseases for micro glial project and tissue replacement 38:00 Amyloid-beta aggregates relate to neurodegeneration FANQ 39:55 Replace the whole brain 42:30 Staging the replacement of the brain over time / process for replacement 44:30 Microrobots / microsurgery option 45:40 Mice model / adapting to intervention 48:18 Optimal time to apply the rejuvenation technology 51:40 Any other way to achieve the result hes going for outside of his approaches 54:00 Viewpoint on the role of the extracellular matrix (ECM) in the damage that needs to be addressed (FANQ) 57:30 Thermodynamic Theory of Aging (FAN Q) 59:59 Other startups being spun out of lab FANQ 01:01:00 People he is on the lookout for 01:02:24 Building in Midwest or staying in NYC 01:03:00 Book recommendations 01:03:30 how to get involved 01:05:40 Self taught people / coders/ etc finding a way to be helpful 01:07:00 Non surgical methods of tissue replacement FANq 01:09:30 Layering the cells for replacement
Dr. Sonia Mayoral is the Robert J. and Nancy D. Carney Assistant Professor of Brain Science at Brown University. In the lab, Sonia studies glial cells, the cells in your brain that aren't neurons. These cells perform a lot of different functions and could hold promise for developing therapies for neurologic diseases. Outside of work, Sonia loves spending as much time as possible with her four-year-old son. Lately, they've been enjoying playing Plants vs. Zombies on the iPad and also acting the game out around the house. She received her bachelor's degree in biological sciences from San Jose State University and her PhD in neuroscience from Stanford University. Afterwards, she conducted postdoctoral research at the University of California, San Francisco. She joined the faculty at Brown University in 2021. In this interview, she shares more about her life and science.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.25.550402v1?rss=1 Authors: Lowenstein, E. D., Misios, A., Buchert, S., Ruffault, P.-L. Abstract: The vagal ganglia, comprised of the superior (jugular) and inferior (nodose) ganglia of the vagus nerve, receive somatosensory information from the head and neck, or viscerosensory information from the inner organs, respectively. Developmentally, the cranial neural crest gives rise to all vagal glial cells and to neurons of the jugular ganglia, while the epibranchial placode gives rise to neurons of the nodose ganglia. Crest-derived nodose glial progenitors can additionally generate autonomic neurons in the peripheral nervous system, but how these progenitors generate neurons is unknown. Here, we found that some Sox10+ neural crest-derived cells in, and surrounding, the nodose ganglion transiently expressed Phox2b, a master regulator of autonomic nervous system development, during early embryonic life. Our genetic lineage tracing analysis revealed that despite their common developmental origin and extreme spatial proximity a substantial proportion of glial cells in the nodose, but not in the neighboring jugular ganglia, have a history of Phox2b expression. Lastly, we used single cell RNA-sequencing (scRNA-seq) to demonstrate that these progenitors give rise to all major glial subtypes in the nodose ganglia, including Schwann cells, satellite glia and glial precursors, and mapped their spatial distribution by in situ hybridization. Our work demonstrates that these crest-derived nodose glial progenitors transiently express Phox2b, give rise to the entire complement of nodose glial cells and display a transcriptional program that may underlie their bipotent nature. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.14.549007v1?rss=1 Authors: Niu, C., Yue, X., An, J. J., Xu, H., Xu, B. Abstract: The brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin-related kinase receptor B (TrkB) are widely expressed in the central nervous system. It is well documented that neurons express BDNF and full-length TrkB (TrkB.FL), and a lower level of truncated TrkB (TrkB.T). With conflicting results, glial cells also have been reported to express BDNF and TrkB. In the current study, we employed a more sensitive and reliable genetic method to characterize the expression of BDNF and TrkB in glial cells in the mouse brain. We utilized three Cre mouse strains in which Cre recombinase is expressed in the same cells as BDNF, TrkB.FL, or all TrkB isoforms, and crossed them to Cre-dependent EGFP reporter mice to label BDNF- or TrkB- expressing cells. We performed immunohistochemistry with glial cell markers to examine the expression of BDNF and TrkB in microglia, astrocytes, and oligodendrocytes. Surprisingly, we found no BDNF- or TrkB- expressing microglia in the brain and spinal cord. Consistent with previous studies, most astrocytes only express TrkB.T in the adult brain. Moreover, there are a small number of astrocytes and oligodendrocytes that express BDNF, the function of which is to be determined. We also found that oligodendrocyte precursor cells, but not mature oligodendrocytes, express both TrkB.FL and TrkB.T in the adult brain. These results not only clarify the expression of BDNF and TrkB in glial cells, but also open opportunities to investigate previously unidentified roles of BDNF and TrkB in glial cells. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.11.548638v1?rss=1 Authors: Kasanga, E. A., Soto, I., Centner, A., McManus, R., Shifflet, M. K., Navarrete, W., Han, Y., Lisk, J., Wheeler, K., Mhatre-Winters, I., Richardson, J. R., Bishop, C., Nejtek, V. A., Salvatore, M. F. Abstract: Background: Alleviation of motor impairment by aerobic exercise (AE) in Parkinsons disease (PD) points to a CNS response that could be targeted by therapeutic approaches, but recovery of striatal dopamine (DA) or tyrosine hydroxylase (TH) has been inconsistent in rodent studies. Objective: To increase translation of AE, 3 components were implemented into AE design to determine if recovery of established motor impairment, concomitant with greater than 80% striatal DA and TH loss, was possible. We also evaluated if serum levels of neurofilament light (NfL) and glial fibrillary acidic protein (GFAP), blood-based biomarkers of disease severity in human PD, were affected. Methods: We used a 6-OHDA hemiparkinson rat model featuring progressive nigrostriatal neuron loss over 28 days, with impaired forelimb use 7 days post-lesion, and hypokinesia onset 21 days post-lesion. After establishing forelimb use deficits, moderate intensity AE began 1-3 days later, 3x per week, for 40 min/session. Motor assessments were conducted weekly for 3 wks, followed by determination of striatal DA, TH protein and mRNA, and NfL and GFAP serum levels. Results: Seven days after 6-OHDA lesion, recovery of depolarization-stimulated extracellular DA and DA tissue content was less than 10%, representing severity of DA loss in human PD, concomitant with 50% reduction in forelimb use. Despite severe DA loss, recovery of forelimb use deficits and alleviation of hypokinesia progression began after 2 weeks of AE and was maintained. Increased NfLand GFAP levels from lesion were reduced by AE. Despite these AE-driven changes, striatal DA tissue and TH protein levels were unaffected. Conclusions: This proof-of-concept study shows AE, using exercise parameters within the capabilities most PD patients, promotes recovery of established motor deficits in a rodent PD model, concomitant with reduced levels of blood-based biomarkers associated with PD severity, without commensurate increase in striatal DA or TH protein. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
You asked, we're here to answer! On this episode of The Social Brain, we will be addressing questions about all things neuroscience sent to us by viewers like you. Be sure to join in and leave any questions you have for future AMA episodes in the comments or the live chat!
Dr. Benjamin Greenberg joined Dr. GG deFiebre of SRNA on our podcast series, “Ask the Expert: Research Edition.” This episode is titled “Update: Study to Investigate the Safety of the Transplantation of Human Glial Restricted Progenitor Cells into Patients with Transverse Myelitis.” Dr. Greenberg discussed the background and status of the study. It is the first of its kind to look at the potential use of stem cells to repair the damage in spinal cords affected by myelitis, inflammation in the spinal cord. He also explained the screening process, enrollment, and next steps of the study.
What a combo of insight and humility is Melissa. I know, that sounds like the first line of a sonnet - she and I tend toward the childlike and the fun. In our time with microphones, we explore -The Rat TicklerWhat's my Cat Hair?Math tests and egg timers"I don't just hire people who are smarter than me, I listen to them."Glial cells - the day shift and the night shiftCortisol overproduction and brain cell erosion - and then we get down to some serious stuff. Please join us as we hike within that three-pound wrinkly mass between your ears.
STRONGER BONES LIFESTYLE: REVERSING THE COURSE OF OSTEOPOROSIS NATURALLY
Have you experienced Restless Leg Syndrome? Today on the Stronger Bones Lifestyle Podcast Debi welcomes back Dr. Loren Fishman to discuss Restless Leg Syndrome. Dr. Fishman has used Yoga as a treatment for women in their 60's who have reversed bone loss without medication or nutritional intervention. In this episode Dr. Fishman and Debi talk about some of the reasons why Restless Leg Syndrome may occur and the ways you can help it stop including a cure Dr Fishman has used on many patients.Key Takeaways:[2:08] What is Restless Leg Syndrome[2:54] A cure for Restless Leg Syndrome[5:56] What is the placebo response[7:17] Dopamine[7:45] Meditation for Restless Leg Syndrome[8:16] Unusual yoga effects[9:04] Minerals and Restless Leg Syndrome[11:46] Gut health and Restless Leg Syndrome[13:57] Sleep and Restless Leg Syndrome[15:55] Mantra[19:48] Looking for a pill[23:07] Restless mind syndrome[24:49] Glial cells and sleepWhere to Find Guest:Sciatica.orgmanhattanphysicalmedicine.com12 Poses vs Osteoporosis Yoga for OsteoporosisMemorable Quotes:"The intestine is the greatest endocrine organ in our bodies, I'm not talking about what it secretes into its own tube, I'm talking about what it secretes outwards to the systemic circulation. There's so many hormones that come out of it, they don't even have names for them, they call them “M” “L” “R”…And they have fabulous effects on everything, only on everything." [12:26] - Dr. Fishman"Sleep is like giving your brain a bath-DebiExactly and then you let the water out of the bath. The brain stays and the water goes." [26:23] -Dr. Fishman To learn more about me and to stay connected, click on the links below:Instagram: @debirobinsonwellnessWebsite: DebiRobinson.comHealthy Gut Healthy Bones ProgramCultural Immersion to Bali 2023
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.05.04.539439v1?rss=1 Authors: Krupp, S., Tam, O., Hammell, M. G., dubnau, j. Abstract: Accumulation of cytoplasmic inclusions of TAR-DNA binding protein 43 (TDP-43) is seen in both neurons and glia in a range of neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimers disease (AD). Disease progression involves non-cell autonomous interactions among multiple cell types, including neurons, microglia and astrocytes. We investigated the effects in Drosophila of inducible, glial cell type-specific TDP-43 overexpression, a model that causes TDP-43 protein pathology including loss of nuclear TDP-43 and accumulation of cytoplasmic inclusions. We report that TDP-43 pathology in Drosophila is sufficient to cause progressive loss of each of the 5 glial sub-types. But the effects on organismal survival were most pronounced when TDP-43 pathology was induced in the perineural glia (PNG) or astrocytes. In the case of PNG, this effect is not attributable to loss of the glial population, because ablation of these glia by expression of pro-apoptotic reaper expression has relatively little impact on survival. To uncover underlying mechanisms, we used cell-type-specific nuclear RNA sequencing to characterize the transcriptional changes induced by pathological TDP-43 expression. We identified numerous glial cell-type specific transcriptional changes. Notably, SF2/SRSF1 levels were found to be decreased in both PNG and in astrocytes. We found that further knockdown of SF2/SRSF1 in either PNG or astrocytes lessens the detrimental effects of TDP-43 pathology on lifespan, but extends survival of the glial cells. Thus TDP-43 pathology in astrocytes or PNG causes systemic effects that shorten lifespan and SF2/SRSF1 knockdown rescues the loss of these glia, and also reduces their systemic toxicity to the organism. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.09.536190v1?rss=1 Authors: Wang, Y., Zhang, R., Huang, S., Valverde, P. T.-T., Lobb-Rabe, M., Ashley, J., Venkatasubramanian, L., Carrillo, R. A. Abstract: Neuronal cell death and subsequent brain dysfunction are hallmarks of aging and neurodegeneration, but how the nearby healthy neurons (bystanders) respond to the cell death of their neighbors is not fully understood. In the Drosophila larval neuromuscular system, bystander motor neurons can structurally and functionally compensate for the loss of their neighbors by increasing their axon terminal size and activity. We termed this compensation as cross-neuron plasticity, and in this study, we demonstrated that the Drosophila engulfment receptor, Draper, and the associated kinase, Shark, are required in glial cells. Surprisingly, overexpression of the Draper-I isoform boosts cross-neuron plasticity, implying that the strength of plasticity correlates with Draper signaling. Synaptic plasticity normally declines as animals age, but in our system, functional cross-neuron plasticity can be induced at different time points, whereas structural cross-neuron plasticity can only be induced at early stages. Our work uncovers a novel role for glial Draper signaling in cross-neuron plasticity that may enhance nervous system function during neurodegeneration and provides insights into how healthy bystander neurons respond to the loss of their neighboring neurons. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.07.536014v1?rss=1 Authors: Kuhn, M. K., Fleeman, R. M., Beidler, L. M., Snyder, A. M., Chan, D. C., Proctor, E. A. Abstract: Introduction: Neuroinflammation and metabolic dysfunction are early alterations in Alzheimer's disease brain that are thought to contribute to disease onset and progression. Glial activation due to protein deposition results in cytokine secretion and shifts in brain metabolism, which have been observed in Alzheimer's disease patients. However, the mechanism by which this immunometabolic feedback loop can injure neurons and cause neurodegeneration remains unclear. Methods: We used Luminex XMAP technology to quantify hippocampal cytokine concentrations in the 5xFAD mouse model of Alzheimer's disease at milestone timepoints in disease development. We used partial least squares regression to build cytokine signatures predictive of disease progression, as compared to healthy aging in wild-type littermates. We applied the disease-defining cytokine signature to wild-type primary neuron cultures and measured downstream changes in gene expression using the NanoString nCounter system and mitochondrial function using the Seahorse Extracellular Flux live-cell analyzer. Results: We identified a pattern of up-regulated IFNgamma, IP-10, and IL-9 as predictive of advanced disease. When healthy neurons were exposed to these cytokines in proportions found in diseased brain, gene expression of mitochondrial electron transport chain complexes, including ATP synthase, was suppressed. In live cells, basal and maximal mitochondrial respiration were impaired following cytokine stimulation. Conclusions: An Alzheimer's disease-specific pattern of cytokine secretion reduces expression of mitochondrial electron transport complexes and impairs mitochondrial respiration in healthy neurons. We establish a mechanistic link between disease-specific immune cues and impaired neuronal metabolism, potentially causing neuronal vulnerability and susceptibility to degeneration in Alzheimer's disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Ariel K. Frame, PhD Candidate in the Neuroscience program at Western University, London, Canada, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 4, entitled, “Aging and memory are altered by genetically manipulating lactate dehydrogenase in the neurons or glia of flies.” DOI - https://doi.org/10.18632/aging.204565 Corresponding authors - Ariel K. Frame - aframe@uwo.ca, and Robert C. Cumming - rcummin5@uwo.ca Abstract The astrocyte-neuron lactate shuttle hypothesis posits that glial-generated lactate is transported to neurons to fuel metabolic processes required for long-term memory. Although studies in vertebrates have revealed that lactate shuttling is important for cognitive function, it is uncertain if this form of metabolic coupling is conserved in invertebrates or is influenced by age. Lactate dehydrogenase (Ldh) is a rate limiting enzyme that interconverts lactate and pyruvate. Here we genetically manipulated expression of Drosophila melanogaster lactate dehydrogenase (dLdh) in neurons or glia to assess the impact of altered lactate metabolism on invertebrate aging and long-term courtship memory at different ages. We also assessed survival, negative geotaxis, brain neutral lipids (the core component of lipid droplets) and brain metabolites. Both upregulation and downregulation of dLdh in neurons resulted in decreased survival and memory impairment with age. Glial downregulation of dLdh expression caused age-related memory impairment without altering survival, while upregulated glial dLdh expression lowered survival without disrupting memory. Both neuronal and glial dLdh upregulation increased neutral lipid accumulation. We provide evidence that altered lactate metabolism with age affects the tricarboxylic acid (TCA) cycle, 2-hydroxyglutarate (2HG), and neutral lipid accumulation. Collectively, our findings indicate that the direct alteration of lactate metabolism in either glia or neurons affects memory and survival but only in an age-dependent manner. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204565 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, astrocyte-neuron lactate shuttle (ANLS), lactate, lactate dehydrogenase, dLdh, Drosophila melanogaster, glia, long-term memory, courtship conditioning About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.18.533255v1?rss=1 Authors: Ray, S., Gurung, P., Manning, R. S., Kravchuk, A., Singhvi, A. Abstract: Each glia interacts with multiple neurons, but the fundamental logic of whether it interacts with all equally remains unclear. We find that a single sense-organ glia modulates different contacting neurons distinctly. To do so, it partitions regulatory cues into molecular microdomains at specific neuron contact-sites, at its delimited apical membrane. For one glial cue, K/Cl transporter KCC-3, microdomain-localization occurs through a two-step, neuron-dependent process. First, KCC-3 shuttles to glial apical membranes. Second, some contacting neuron cilia repel it, rendering it microdomain-localized around one distal neuron-ending. KCC-3 localization tracks animal aging, and while apical localization is sufficient for contacting neuron function, microdomain-restriction is required for distal neuron properties. Finally, we find the glia regulates its microdomains largely independently. Together, this uncovers that glia modulate cross-modal sensor processing by compartmentalizing regulatory cues into microdomains. Glia across species contact multiple neurons and localize disease-relevant cues like KCC-3. Thus, analogous compartmentalization may broadly drive how glia regulate information processing across neural circuits. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.14.532493v1?rss=1 Authors: Cheng, Y.-T., Luna-Figueroa, E., Woo, J., Chen, H.-C., Lee, Z.-F., Harmanci, A. S., Deneen, B. Abstract: Communication between neurons and glia plays an important role in establishing and maintaining higher order brain function. Astrocytes are endowed with complex morphologies which places their peripheral processes in close proximity to neuronal synapses and directly contributes to their regulation of brain circuits. Recent studies have shown that excitatory neuronal activity promotes oligodendrocyte differentiation; whether inhibitory neurotransmission regulates astrocyte morphogenesis during development is unknown. Here we show that inhibitory neuron activity is necessary and sufficient for astrocyte morphogenesis. We found that input from inhibitory neurons functions through astrocytic GABABR and that its deletion in astrocytes results in a loss of morphological complexity across a host of brain regions and disruption of circuit function. Expression of GABABR in developing astrocytes is regulated in a region-specific manner by SOX9 or NFIA and deletion of these transcription factors results in region-specific defects in astrocyte morphogenesis, which is conferred by interactions with transcription factors exhibiting region-restricted patterns of expression. Together our studies identify input from inhibitory neurons and astrocytic GABABR as universal regulators of morphogenesis, while further revealing a combinatorial code of region-specific transcriptional dependencies for astrocyte development that is intertwined with activity-dependent processes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.24.529840v1?rss=1 Authors: Koupourtidou, C., Schwarz, V., Aliee, H., Frerich, S., Fischer-Sternjak, J., Bocchi, R., Simon-Ebert, T., Dichgans, M., Goetz, M., Theis, F. J., Ninkovic, J. Abstract: Traumatic brain injury leads to a highly orchestrated immune- and glial cell response partially responsible for long-lasting disability and the development of secondary neurodegenerative diseases. A holistic understanding of the mechanisms controlling the responses of specific cell types and their crosstalk is required to develop an efficient strategy for better regeneration. Here, we combined spatial and single-cell transcriptomics to chart the transcriptomic signature of the injured murine cerebral cortex, and identified specific states of astrocytes, microglia, and oligodendrocyte precursor cells contributing to this signature. Interestingly, these cellular populations share a large fraction of injury-regulated genes, including inflammatory programs downstream of the innate immune-associated pathways Cxcr3 and Tlr1/2. Systemic manipulation of these pathways decreased the reactivity state of glial cells associated with poor regeneration. The functional relevance of the newly discovered shared signature of glial cells highlights the importance of our resource enabling comprehensive analysis of early events after brain injury. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.15.528337v1?rss=1 Authors: Toro, C. A., Johnson, K. E., Hansen, J., Siddiq, M. M., Vasquez, W., Zhao, W., Graham, Z. A., Saez, J. C., Iyengar, R., Cardozo, C. P. Abstract: Membrane channels such as connexins (Cx), pannexins (Panx) and P2X7 receptors (P2X7R) are permeable to calcium ions and other small molecules such as ATP and glutamate. Release of ATP and glutamate through these channels is a key mechanism driving tissue response to traumas such as spinal cord injury (SCI). Boldine, an alkaloid isolated from the Chilean boldo tree, blocks both Cx hemichannels (HC) and Panx. To test if boldine could improve function after SCI, boldine or vehicle was administered to treat mice with a moderate severity contusion-induced SCI. Boldine led to greater spared white matter and increased locomotor function as determined by the Basso Mouse Scale and horizontal ladder rung walk tests. Boldine treatment reduced immunostaining for markers of activated microglia (Iba1) and astrocytic (GFAP) markers while increasing that for axon growth and neuroplasticity (GAP-43). Cell culture studies demonstrated that boldine blocked glial HC, specifically Cx26 and Cx30, in cultured astrocytes and blocked calcium entry through activated P2X7R. RT-qPCR studies showed that boldine treatment reduced expression of the chemokine Ccl2, cytokine IL-6 and microglial gene CD68, while increasing expression of the neurotransmission genes Snap25 and Grin2b, and Gap-43. Bulk RNA sequencing (of the spinal cord revealed that boldine modulated a large number of genes involved in neurotransmission in in spinal cord tissue just below the lesion epicenter at 14 days after SCI. Numbers of genes regulated by boldine was much lower at 28 days after injury. These results indicate that boldine treatment ameliorates injury and spares tissue to increase locomotor function. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
When you think of brain cells, you probably think of neurons. That's perfectly understandable. Discussions of the brain almost always focus on neurons. But there is another family of brain cells, (glial cells) that, by some estimates, outnumber neurons by 10 to 1!. Even if the the percentage is more like 50/50, that's a lot of cells - billions!Based on what I have read, I have a sneaking suspicion that glial cells are in charge of the brain! Yup. Neurons are the work horses, but glial cells hold the reins. In this episode, I discuss the mysteries of glial cells with Dr. Jeff Darling. We discuss the four basic types of glial cells and what they do - and why I think they are running the show. Click on Chapters (above) to see specific topic ares. Support the showSupport our work to promote creative aging. Subscribe to the MINDRAMP Podcast.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526565v1?rss=1 Authors: Stepankova, K., Chudickova, M., Simkova, Z., Martinez-Varea, N., Kubinova, S., Urdzikova, L., Jendelova, P., Kwok, J. C. F. Abstract: Following a spinal cord injury (SCI), chondroitin sulfate proteoglycans (CSPGs) are up-regulated at the glial scar inhibiting neuroregeneration. Under normal physiological condition, CSPGs interact with hyaluronan (HA) and other extracellular matrix on neuronal surface forming a macromolecular structure called perineuronal nets (PNNs) which regulate neuroplasticity. 4-methylumbelliferone (4-MU) has been used previously to down-regulate HA synthesis but not been tested in SCI. In this study, we have evaluated the effect of 4-MU, an inhibitor of HA, in a chronic contusion model of SCI in rats. At a dose of 1.2 g/kg/day of 4-MU, we observed not only the reduction of HA in the uninjured spinal cords after 60 days of 4-MU administration, but also a down-regulation of CS glycosaminoglycans (CS-GAGs). In order to assess the effect of 4-MU in chronic SCI, rats with T8 spinal contusion injury were fed with 4-MU or placebo for 8 weeks in combination with daily treadmill rehabilitation for 16 weeks to promote neuroplasticity. 4-MU treatment promoted significant sprouting of 5-hydroxytryptamine (5-HT) positive fibres into ventral horns and reduced the HA synthesis by astrocytes around the lesion site. While 4-MU reduced astrogliosis in chronic stage of SCI, the current dose was not sufficient to down-regulate the increased production of CS-GAGs or behavioural performance. Together, these data suggest that oral treatment with 4-MU is able to induce anatomical plasticity but further adjustment on the dosage will be required to benefit functional recovery after SCI. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Louisa Nicola is a neurophysiologist and brain coach for many professional athletes and Wall Street execs. She discusses science-based tools and strategies to boost brain health and mental performance. Support your Workout Sessions and Healthy Hydration with this Creatine Electrolyte Combo by MYOXCIENCE Save 15% with code podcast at checkout Link to the Video Interview: https://bit.ly/3R7noel Connect with Louisa: https://www.neuroathletics.com.au Show Notes: 03:10 Louisa was elite triathlete when she realized the impact the brain had on all aspects of performance. She and her fellow athletes were not taught about sleep or nutrition. 04:20 The nervous system must be optimized to optimize performance throughout the body and as a person. 05:35 We used to sleep about 12 hours a day in prehistoric times. Sleep regenerates our brains. 06:20 There are 4 stages of sleep. Stage one is as you are falling asleep. Stage 2 is light sleep. Stage 3 is deep sleep/slow wave sleep/non-REM sleep. Stage 4 is REM sleep. Stages 3 and 4 are the most important stages for our brains. 06:52 During deep sleep, hormones are secreted: testosterone, estrogen, growth hormone. The glymphatic system is your brains sewage system. It cleans toxins, including amyloid beta. A buildup of these toxins can lead to neurodegenerative diseases. 07:50 Your brain is comprised of neurons and others. Glial cells bind neurons together. During deep sleep, glial cells shrink, making way for the cerebral spinal fluid in your brain to wash out the trash. 08:55 A groggy wakeup may be an indication that you are not getting into deep sleep. 30% of your total sleep time should be deep sleep. 20% of total sleep time should be REM sleep. 09:30 REM sleep is where memory consolidation and learning take place. 10:30 The biggest disruptor of sleep is anxiety and stress. This activation of the sympathetic nervous system may prevent you from falling asleep or wake you in the night. 10:55 Alcohol is the biggest inhibitor of REM sleep. Blue light blocking glasses are helpful, but do not block out all light. 12:00 Eating less than 2 hours before bed keeps us awake through digestion and the increase in our core body temperature. Core body temperature must drop at least 2 degrees for us to go to sleep and stay asleep. 15:00 Alcohol inhibits the action of GABA, our calming neurotransmitter. Cortisol peaks with alcohol. Alcohol and marijuana sedate you. It does not elicit sleep stages. 16:15 You are preparing for sleep the minute you wake up. Consistency is key. 17:20 Try to get as much sleep as possible before you get on a plane. It is called Sleep Banking. 18:10 Your prefrontal cortex is the ruler of your brain. It is where cognition happens: attention, reaction time, processing speed. 6 hours of sleep is a sleep deprived state, in the scientific literature. 10:20 As we age, we have a lower efficacy of our frontal lobe. There is a thinning of our cerebral cortex. Thinning in the prefrontal cortex causes a lower decision rate and worsening of our processing speed, inhibition and impulse control. 21:20 We can slow brain ageing through lifestyle interventions, such as sleep, good nutrition and exercise. 21:40 There is an atrophy of our brain white matter, where our myelinated neurons live, as we get older. Our processing speed declines. This can be seen using an EEG. 25:50 Mild cognitive impairment is a predementia state. 27:30 You should be working on your brain. It is the control center of your entire body. 27:50 You can stave off predementia states and the slowing of cognition through exercise. 29:45 Head trauma can cause an accumulation of talc proteins tolC proteins and amyloid beta, which is somewhat comparable to Alzheimer's disease. 30:30 A hard hit may require a month's recovery. Within 24 hours post trauma, decreasing the temperature of the brain, eating a high fat diet, or having exogenous ketones can help heal the brain. 33:40 Ingesting exogenous ketones can help prevent trauma from happening to the brain. 36:00 EPA/DHA are anti-inflammatory. If you have a high omega 3 index of 8% or more, you can increase your life expectancy by 5 years. 37:10 A risk factor for all-cause mortality is a low omega 3 index. 37:40 Quality supplements reduce risk of oxidation and toxicity. EPA/DHA feeds your brain what it is made of. It is made of water and fat. A high omega 3 index helps with cell membrane fluidity. 39:25 A standard omega 3 blood panel does not test the red blood cell. Red blood cell cycle lasts about 120 days. You need to ingest EPA/DHA daily for cardiac, brain and overall health. 41:20 Farm raised seafood does not contain the same amount of nutrients. 41:30 Omega 3 is made of EPA, DHA and ALA. ALA is the plant form found in flax and chia seeds. To get the recommended dose of omega 3 through ALA is a lot of food. ALA gets converted into DHA. 42:20 Your eyes are the only neurologic tissue outside your brain. Vision changes may be a way to indirectly assess brain health. 45:05 Most 2019 deaths were attributable to heart disease and brain diseases. 45:40 A healthy performing brain can make sound decisions, be rational and practice impulse control. 47:00 Your brain fatigues faster if you are not eating well, sleeping well, and exercising. You need brain energy. Stress and an inflamed brain disrupts pathways in the brain. 48:50 People who have type 2 diabetes and obesity have a higher rate of neural inflammation. 49:50 When we exercise there is a release of myokines, muscle-based proteins (peptide hormones). They act on different organs in positive ways. They are water soluble, and some can pass the blood-brain barrier. Binding receptors to myokines are on heart muscle, spleen, liver and more. Once bound, they create a chemical reaction. 51:10 Interleukin 6 myokine, is secreted with the contraction of a muscle. It is pro-inflammatory cytokine… unless it is released from a muscle – where it is released as anti-inflammatory. It affects immunity and different areas of the brain. 52:00 Irisin myokine is a messenger molecule. It crosses the blood-brain barrier to the prefrontal cortex, where it affects cognition, and hippocampus, where it induces BDNF, that induces neurogenesis. 53:56 When you learn something and immediately exercise, you can have greater capacity to remember. If you sleep for 20 minutes after learning something, you will embed everything you learned. 54:30 Irisin release is increased 1 hour after exercise. 54:50 Workouts of 70 to 80% of you one rep max for a robust release of irisin. More of a release is given during resistance training, than aerobic. The more resistance, the more the release. 58:10 You can stave of neurodegenerative diseases and states by 20 years by inducing exercise protocols that impact myokine release. 58:50 50 million people worldwide are affected by Alzheimer's disease. That rate is set to triple by 2050. 59:30 EPA/DHA can clear accumulated proteins in your brain. 00:01:00 Demyelinating diseases, MS, are becoming more prevalent. Chronic stress and chronic cortisol may be the cause.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.09.523229v1?rss=1 Authors: Rey, S., Ohm, H., Moschref, F., Zeuschner, D., Klämbt, C. Abstract: Neuronal information conductance depends on transmission of action potentials. The conductance of action potentials is based on three physical parameters: The axial resistance of the axon, the axonal insulation by glial membranes, and the positioning of voltage-gated ion channels. In vertebrates, myelin and channel clustering allow fast saltatory conductance. Here we show that in Drosophila melanogaster voltage-gated sodium and potassium channels, Para and Shal, co-localize and cluster in an area of motor axons resembling the axon initial segment. Para but not Shal localization depends on peripheral glia. In larvae, relatively low levels of Para channels are needed to allow proper signal transduction and nerves are simply wrapped by glial cells. In adults, the concentration of Para at the axon initial segment increases. Concomitantly, these axon domains are covered by a mesh of glial processes forming a lacunar structure that serves as an ion reservoir. Directly flanking the voltage-gated ion channel rich axon segment, the lacunar structures collapse forming a myelin-like insulation. Thus, Drosophila development may reflect the evolution of myelin which forms in response to increased levels of clustered voltage-gated ion channels. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.26.521704v1?rss=1 Authors: Martin, C. G., Bent, J. S., Singhvi, A. Abstract: For an organ to maintain proper architecture and function, its different component cell-types must coordinate their cell-shapes with each other through life. While cell-intrinsic developmental mechanisms driving homotypic cell-cell coordination are known, how heterotypic cells collectively regulate cell-shape is less-clear. We report that, in a sense-organ, epithelial cells delimit and maintain polarity domains of contacting glia, and thereby, associated neuron shapes throughout life. Briefly, Hsp co-chaperone UNC-23/BAG2 keeps epithelial apical domains from deforming with animal movement. Epithelial apical domains stretch aberrantly and progressively in adult unc-23 mutant animals, which in an FGFR-dependent manner, dislocates glial apical cytoskeleton proteins SMA-1/{beta}H-Spectrin and actin. This alters glial apical polarity and cell shape, and concomitantly, associated neuron-ending shape. Notably, UNC-23 acts temporally at a developmental critical period to maintain glia-neuron shape in adults, and spatially within a defined anatomical zone. Lastly, intervention in either epithelia, glia or neuron ameliorate or phenocopy unc-23 neural defects. Epi/endothelia resist mechanical stress and contact glia-neuron units across central/peripheral nervous systems and species, and all components of the identified molecular pathway are conserved and disease-relevant. Thus, we posit that analogous epithelia-glia mechanobiological coupling may broadly regulate glia-neuron shapes through animal life. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.16.520775v1?rss=1 Authors: Perron, C., Carme, P., Llobet Rosell, A., Minnaert, E., Ruiz Demoulin, S., Szczkowski, H., Neukomm, L. J., Dura, J.-M., Boulanger, A. Abstract: During animal development, neurons often form exuberant or incorrect axons and dendrites at early stages, followed by the refinement of neuronal circuits at late stages. Neural circuit refinement leads to the production of large amounts of neuronal debris in the form of neuronal cell corpses, fragmented axons and dendrites, and pruned synapses requiring disposal. In particular, the predominant phagocytes acting during the neuronal remodeling and degeneration are glial cells and critical signaling pathways between neurons and glia leading to phagocytosis are required. Chemokine-like mushroom body neuron secreted Orion ligand was shown to be essential to the astrocyte infiltration into the {gamma} axon bundle leading to {gamma} axon pruning and clearance of debris left from axon fragmentation. Here we show a role of orion also in debris engulfment and phagocytosis. Interestingly, we show that orion is also involved in the overall transformation of astrocytes into phagocytes. In addition, analysis of several neuronal paradigms demonstrates the role of orion in the elimination of both peptidergic vCrz+ and PDF-Tri neurons via additional phagocytic glial cells as cortex and/or ensheathing glia. Our results suggest that Orion is essential for phagocytic activation of three different types of glial cells: astrocytes, cortex and ensheathing glia and point to Orion as a trigger not only of glial infiltration but also engulfment and phagocytosis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.15.520639v1?rss=1 Authors: Metcalf, M. G., Monshietehadi, S., Sahay, A., Frakes, A. E., Durieux, J., Velichkovska, M., Mena, C., Farinas, A., Sanchez, M., Dillin, A. Abstract: Glia are the protectors of the nervous system, providing neurons with support and protection from cytotoxic insults. We previously discovered that four astrocyte-like glia can regulate organismal proteostasis and longevity in C. elegans. Expression of the UPRER transcription factor, XBP-1s, in these glia increases stress resistance, longevity, and activates the UPRER in intestinal cells via neuropeptides. Autophagy, a key regulator of metabolism and aging, has been described as a cell autonomous process. Surprisingly, we find that glial XBP-1s enhances proteostasis and longevity by cell non-autonomously reprogramming organismal lipid metabolism and activating autophagy. Glial XBP-1s regulates the activation of another transcription factor, HLH-30/TFEB, in the intestine. HLH-30 activates intestinal autophagy, increases intestinal lipid catabolism, and upregulates a robust transcriptional program. Our study reveals a novel role for glia in regulating peripheral lipid metabolism, autophagy, and organellar health through peripheral activation of HLH-30 and autophagy. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
10 Ways to Clean Up Your Brain - Glymphatic SystemIn this podcast, Dr. Rodney and Karen talk about the glymphatic system. What is the glymphatic system?Your Central Nervous System is highly active so metabolic waste can build up quickly. It is also very sensitive to fluctuations in its environment, so the body needs to remove cellular garbage somehow, and that's where the glymphatic system comes in.Before the discovery of this brain-based garbage disposal system, scientists believed that each individual cell handled its own metabolic waste.Why is the system called the glymphatic system?The name is a reference to the glial cells, which are vital to this waste clearance system.Glial cells get relatively little coverage, compared with neurons, despite being just as numerous in the brain. They were long considered little more than lowly support cells, but are now held in higher regard.Glia protect, nourish, and insulate neurons. They also play a role in the immune system and, as we now know, the glymphatic system.The glymphatic system, which runs parallel to arteries, also harnesses the pulsing of blood in circulation to help keep things moving.As the blood vessels expand rhythmically, they drive the exchange of compounds between the interstitial space and the CSF(clean cerebrospinal fluid) which replaces the waste productsThe glymphatic system connects with the lymphatic system of the rest of the body at the dura, a thick membrane of connective tissue that covers the CNS. The lymphatic system gets rid of the toxins, waste and other unwanted material.Why is the glymphatic system so important?If the cellular system became overloaded or slowed down as we aged, metabolic garbage would build up between the cells. This garbage includes products such as beta-amyloid — the protein associated with Alzheimer's disease.It is important to keep this metabolic waste from accumulating in the brain.Brain cells perform autophagy (“self eating”) to scavenge additional waste by mopping up diseased and damaged bits of tau protein and beta-amyloid.What are causes of glymphatic system congestion?Chronic inflammation (Listen to more)Poor sleep quality (Sleep secrets 1)Blood sugar dysregulationChronic stress (Listen to more)Environmental toxinsWhat are some action steps to improve glymphatic flow?Prioritize high quality deep sleep (Sleep Secrets 2)Eat according to an anti-inflammatory nutrition planConsume high levels of omega 3 fatty acidsPractice intermittent fastingSleep on your sideMove and exercise consistentlyGet regular chiropractic careAvoid chronic stressAvoid or reduce alcohol consumptionRed light laser therapyFollow us on Instagram at https://www.instagram.com/stanceforhealthFollow us on Facebook at https://www.facebook.com/stancechiropracticOur website is: https://www.stancechiropractic.com/podcastPlease rate us and write a review!
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.08.519463v1?rss=1 Authors: Vangansewinkel, T., Lemmens, S., Tiane, A., Geurts, N., Dooley, D., Vanmierlo, T., Pejler, G., Hendrix, S. Abstract: Traumatic spinal cord injury (SCI) most often leads to permanent paralysis due to the inability of axons to regenerate in the adult mammalian central nervous system (CNS). In the past, we have shown that mast cells (MCs) improve the functional outcome after SCI by suppressing scar tissue formation at the lesion site via mouse mast cell protease 6 (mMCP6). In this study, we investigated whether recombinant mMCP6 can be used therapeutically to improve the functional outcome after SCI. Therefore, we applied mMCP6 locally via an intrathecal catheter in the subacute phase after a spinal cord hemisection injury in mice. Our findings showed that hind limb motor function was significantly improved in mice that received recombinant mMCP6 compared to the vehicle-treated group. In contrast to our previous findings in mMCP6 knockout mice, the lesion size and expression levels of the scar components fibronectin, laminin, and axon growth-inhibitory chondroitin sulfate proteoglycans were not affected by the treatment with recombinant mMCP6. Surprisingly, no difference in infiltration of CD4+ T cells and reactivity of Iba-1+ microglia/macrophages at the lesion site was observed between the mMCP6 treated mice and control mice. Additionally, local protein levels of the pro- and anti inflammatory mediators IL-1{beta}, IL-2, IL-4, IL-6, IL 10, TNF-, IFN{gamma}, and MCP-1 were comparable between the two treatment groups, indicating that locally applied mMCP6 did not affect inflammatory processes after injury. However, the increase in locomotor performance in mMCP6-treated mice was accompanied by reduced demyelination and astrogliosis in the perilesional area after SCI. Consistently, we found that TNF-a/IL-1B-astrocyte activation was decreased, and that oligodendrocyte precursor cell (OPC) differentiation was increased after recombinant mMCP6 treatment in vitro. Mechanistically, this suggests effects of mMCP6 on reducing astrogliosis and improving (re)myelination in the spinal cord after injury. In conclusion, these data show for the first time that recombinant mMCP6 is therapeutically active in enhancing recovery after SCI. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
The function of microglia and astrocytes in the brain may mediate the intersection of sex-differential biology and autism biology. The post Autism's sex bias tied to glial, immune cell gene expression appeared first on Spectrum | Autism Research News.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.30.518536v1?rss=1 Authors: Gala, D. S., Lee, J. Y., Kiourlappou, M. S., Titlow, J. S., Teodoro, R. O., Davis, I. Abstract: The polarization of cells often involves the transport of specific mRNAs and their localized translation in distal projections. Neurons and glia both contain long cytoplasmic processes with important functions. While mRNA localization has been studied extensively in neurons, little is known in glia, especially in intact nervous systems. Here, we predicted 1700 localized Drosophila glial transcripts by extrapolating from our meta-analysis of 8 existing studies characterizing the localized transcriptomes and translatomes of synaptically-associated mammalian glia. We tested these predictions in glia of the neuromuscular junction of Drosophila larvae and found that localization to vertebrate glia is a strong predictor of mRNA localization of the high confidence Drosophila homologues. We further showed that some of these localized transcripts are required in glia for plasticity of neuromuscular junction synapses. We conclude that peripheral glial mRNA localization is a common and conserved phenomenon and propose that it is likely to be functionally important. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
The function of microglia and astrocytes in the brain may mediate the intersection of sex-differential biology and autism biology.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.26.513909v1?rss=1 Authors: Masrori, P., Bijnens, B., Davie, K., Poovathingal, S. K., Storm, A., Hersmus, N., Fumagalli, L., Van Den Bosch, L., Fiers, M., Thal, D. R., Mancuso, R., Van Damme, P. Abstract: Neuroinflammation is an important hallmark in amyotrophic lateral sclerosis (ALS). Experimental evidence has highlighted a role of microglia in the modulation of motor neuron degeneration. However, the exact contribution of microglia to both sporadic and genetic forms of ALS is still unclear. We generated single nuclei profiles of spinal cord and motor cortex from sporadic and C9orf72 ALS patients, as well as controls. We particularly focused on the transcriptomic responses of both microglia and astrocytes. We confirmed that C9orf72 is highly expressed in microglia and shows a diminished expression in carriers of the hexanucleotide repeat expansion (HRE). This resulted in an impaired response to disease, with specific deficits in phagocytic and lysosomal transcriptional pathways. Astrocytes also displayed a dysregulated response in C9orf72 ALS patients, remaining in a homeostatic state. This suggests that C9orf72 HRE alters a coordinated glial response, which ultimately would increase the risk for developing ALS. Our results indicate that C9orf72 HRE results in a selective microglial loss-of-function, likely impairing microglial-astrocyte communication and preventing a global glial response. This is relevant as it indicates that sporadic and familial forms of ALS may present a different cellular substrate, which is of great importance for patient stratification and treatment. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.19.512981v1?rss=1 Authors: Frame, A. K., Robinson, J. W., Mahmoudzadeh, N. H., Tennessen, J. M., Simon, A. F., Cumming, R. C. Abstract: The astrocyte-neuron lactate shuttle hypothesis posits that glial-generated lactate is transported to neurons to fuel metabolic processes required for long-term memory. Although studies in vertebrates have revealed that lactate shuttling is important for cognitive function, it is uncertain if this form of metabolic coupling is conserved in invertebrates or is influenced by age. Lactate dehydrogenase (Ldh) is a rate limiting enzyme that interconverts lactate and pyruvate. Here we genetically manipulated expression of Drosophila melanogaster lactate dehydrogenase (dLdh) in neurons or glia to assess the impact of altered lactate metabolism on invertebrate aging and long-term courtship memory at different ages. We also assessed survival, negative geotaxis, brain neutral lipids (the core component of lipid droplets) and brain metabolites. Both upregulation and downregulation of dLdh in neurons resulted in decreased survival and memory impairment with age. Glial downregulation of dLdh expression caused age-related memory impairment without altering survival, while upregulated glial dLdh expression lowered survival without disrupting memory. Both neuronal and glial dLdh upregulation increased neutral lipid accumulation. We provide evidence that altered lactate metabolism with age affects the tricarboxylic acid (TCA) cycle, 2-hydroxyglutarate (2HG), and neutral lipid accumulation. Collectively, our findings indicate that the direct alteration of lactate metabolism in either glia or neurons affects memory and survival but only in an age-dependent manner. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.07.511264v1?rss=1 Authors: Jager, S. E., Goodwin, G. L., Chisholm, K. I., Denk, F. Abstract: Satellite glial cells (SGCs) are important for proper neuronal function of primary sensory neurons to whom they provide homeostatic support. Most research of SGC function has been performed with in vitro studies, but recent advances in in vivo calcium imaging and transgenic mouse models have enabled this first study of single cell SGC function in vivo. We found that under most circumstances, SGCs do not respond in a time-locked fashion to neuronal firing. The one exception to this was suprathreshold stimulation of the sciatic nerve, which led to some time-locked signals, but only in painful inflammatory and neuropathic states. Surprisingly therefore, we conclude that most calcium signals in SGCs seem to develop at arbitrary intervals not directly linked to neuronal activity patterns. More in line with expectations, our experiments also revealed that the number of active SGCs was increased under conditions of inflammation or nerve injury. This could reflect the increased requirement for homeostatic support across dorsal root ganglion neuron populations, which are more active during such painful states. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.28.509837v1?rss=1 Authors: Park, S. H. E., Kulkarni, A., Konopka, G. Abstract: During cortical development, human basal radial glial cells (bRGCs) are highly capable of sustained self-renewal and neurogenesis. Selective pressures on this cell type may have contributed to the evolution of the human neocortex, leading to an increase in cortical size. bRGCs have enriched expression for Forkhead Box P1 (FOXP1), a transcription factor implicated in neurodevelopmental disorders such as autism spectrum disorder. However, the cell type-specific roles of FOXP1 in bRGCs during cortical development remain unexplored. Here, we examine the requirement for FOXP1 gene expression regulation underlying the production of bRGCs using human brain organoids. We examine a developmental time point when FOXP1 expression is highest in the cortical progenitors, and the bRGCs, in particular, begin to actively produce neurons. With the loss of FOXP1, we show a reduction in the number of bRGCs, as well as reduced proliferation and differentiation of the remaining bRGCs, all of which lead to reduced numbers of excitatory cortical neurons over time. Using single-nuclei RNA sequencing and cell trajectory analysis, we uncover a role for FOXP1 in directing cortical progenitor proliferation and differentiation by regulating key signaling pathways related to neurogenesis and neurodevelopmental disorders. Together, these results demonstrate that FOXP1 regulates human-specific features in early cortical development. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.19.508484v1?rss=1 Authors: Snellman, A., Ekblad, L. L., Tuisku, J., Koivumäki, M., Ashton, N. J., Lantero-Rodriguez, J., Karikari, T. K., Helin, S., Bucci, M., Löyttyniemi, E., Parkkola, R., Karrash, M., Schöll, M., Zetterberg, H., Blennow, K., Rinne, J. Abstract: Increased reactivity of microglia and astrocytes is known to be present at various stages of the Alzheimer's continuum but their relationship with core Alzheimer's disease pathology in the preclinical stages is less clear. We investigated glial reactivity and {beta}-amyloid pathology in cognitively unimpaired APOE {varepsilon}4 homozygotes, heterozygotes and non-carriers using 11C-PK11195 PET (targeting 18-kDa translocator protein), 11C-PiB PET (targeting {beta}-amyloid), brain MRI, and a preclinical cognitive composite (APCC). Plasma glial fibrillary acidic protein (GFAP) by and plasma A{beta}1-42/1-40 were measured using single molecule array and immunoprecipitation combined with mass spectrometry, respectively. We observed that (i) 11C-PiB-binding was significantly higher in APOE {varepsilon}4 homozygotes compared with non-carriers in all evaluated regions, (ii) regional 11C-PK11195-binding did not differ between the APOE {varepsilon}4 gene doses or between A{beta}-positive and -negative individuals, and (iii) higher 11C-PK11195-binding and plasma GFAP were associated with lower hippocampal volume, and elevated 11C-PiB-binding and plasma GFAP concentration with lower APCC scores. Increased glial reactivity might emerge in later stages of preclinical Alzheimer's disease in parallel with early neurodegenerative changes. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.15.508143v1?rss=1 Authors: Rowland, M. E., Jiang, Y., Shafiq, S., Ghahramani, A., Pena-Ortiz, M. A., Dumeaux, V., Berube, N. G. Abstract: Neurodevelopmental disorders are often characterized by abnormal production of myelin, an extension of the oligodendrocyte plasma membrane wrapped around axons to facilitate nerve conduction. However, the molecular mechanisms that control myelination during brain development are incompletely resolved. Here, we provide evidence that loss of ATRX, encoded by the gene mutated in the ATR-X intellectual disability syndrome, leads to myelin deficits in the mouse CNS. While postnatal systemic thyroxine administration can improve myelination, the rescue is incomplete, pointing to additional roles of ATRX in this process. We show that targeted inactivation of ATRX in postnatal oligodendrocyte progenitor cells (OPCs), but not in neurons, also leads to myelination deficits, demonstrating cell-intrinsic effects of ATRX deficiency. A subset of ATRX-null OPCs express lower levels of oligodendrocyte specification and differentiation markers, including the basic helix-loop-helix Olig2 transcription factor. Mechanistically, we provide evidence that ATRX occupies genomic sites in OPCs marked by H3K27Ac, CHD7 and CHD8 and demonstrate that reduced Olig2 expression is associated with decreased H3K27Ac. Finally, our data suggest that ATRX-null OPCs acquire a more plastic state and can exhibit astrocyte-like features in vitro and in vivo, supporting a model in which ATRX regulates the onset of myelination by promoting OPC identity and suppressing astrogliogenesis. These previously unrecognized functions of ATRX might explain white matter pathogenesis in ATR-X syndrome patients. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.10.507291v1?rss=1 Authors: Boestrand, S. M. K., Seeker, L. A., Kazakou, N.-L., Bestard-Cuche, N., Jaekel, S., Kenkhuis, B., Henderson, N. C., de Bot, S. T., van Roon-Mom, W., Priller, J., Williams, A. Abstract: Huntington's disease (HD) is a severely debilitating, autosomal dominant neurodegenerative disease with a fatal outcome. There is accumulating evidence of a prominent role of glia in the pathology of HD, and we investigated this by conducting single nuclear RNA sequencing (snRNAseq) of human post mortem brain in four differentially affected regions; caudate nucleus, frontal cortex, hippocampus and cerebellum. Across 127,205 nuclei from people with HD, and age/sex matched controls, we found heterogeneity of glia which is altered in HD. We describe prominent changes in the abundance of certain subtypes of astrocytes, microglia, oligodendrocyte precursor cells and oligodendrocytes between HD and control samples, and these differences are widespread across brain regions. Furthermore, we highlight two possible mechanisms that characterise the glial contribution to disease pathology. Firstly, we show that upregulation of molecular chaperones represents a cross-glial signature in HD, which likely reflects an adaptive response to the accumulation of mutant Huntingtin (mHTT). Secondly, we show an oligodendrocyte-specific upregulation of the calmodulin-dependent 3',5'-cyclic nucleotide phosphodiesterase 1A (PDE1A) in HD brain compared to controls, which may cause dysfunction of key cellular functions due to the downregulation of the important second messengers cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Our results support the hypothesis that glia have an important role in the pathology of HD, and show that all types of glia are affected in the disease. As glia are more tractable to treat than neurons, our findings may be of therapeutic relevance. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
In this solo episode, JFOD covers a number of contemporary psychology articles. He comments on pieces about the signs of gaslighting, the signs of Histrionic Personality Disorder, the effect of Glial cells on mood, and whether or not we should pay attention to the news. Support JFOD on Patreon: Patreon.com/jfod. Join JFOD's newsletter: JFODnews.com.
Behind every successful neuron are glial cells. Glial cells are non-neuronal cells. They are a diverse range of cells which allow the neuron to do its job. They provide metabolic support to neurons, including neuronal insulation, communication, nutrient transport and even act as immune support. For instance, issues with microglia (a type of glial cells that is helpful for waste transport/immune support for neurons) has been implicated in Alzheimer's disease. Like what you hear? Spread the word! More information about me: https://linktr.ee/Drbillakotamd --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app
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Dr. Nathan Smith will soon be starting his new roles as Associate Dean for Equity and Inclusion in Research and Research Education as well as Associate Professor of Neuroscience in the School of Medicine and Dentistry at the University of Rochester. Currently, Nathan is Director of Basic Neuroscience Research and a Principal Investigator in the Center for Neuroscience Research at Children's National Research Institute as well as an Assistant Professor of Pediatrics and Pharmacology & Physiology at George Washington University School of Medicine and Health Sciences. Nathan studies a type of cell in the brain that helps the brain perform certain tasks like managing blood flow. These cells also help other cells in the brain, such as neurons, communicate with each other. Nathan focuses particularly on interactions between neurons and glial cells in healthy brains and in models of diseases like ADHD, Depression, and epilepsy. When he's not working in the lab, Nathan enjoys practicing martial arts. He is a black belt in Seidokan Karate, and this has been a passion for Nathan since graduate school that helps him keep his life in balance. He received his B.S. in Biology from Xavier University and his M.S. and Ph.D. in Neuroscience from the University of Rochester School of Medicine and Dentistry. When he graduated in 2013, Nathan was the first African American to receive a Ph.D. in Neuroscience from the University of Rochester. Afterwards, Nathan conducted postdoctoral research at the University of Utah and Boston University, as well as at Children's National Hospital. Nathan has received numerous honors and awards in his career including being named a 2021 Fellow of the American Association for the Advancement of Science (AAAS), receipt of the 2019 Neuroscience Alumni Award from the University of Rochester, and receipt of the 2018 Children's National President's Award for Innovation in Research. In our interview, Nathan shares more about his life and science.
Enjoy this month's collection of fascinating puzzle pieces. We offer new pieces the first week of every month. They may even speak to what puzzles you! Listen to the podcast and download these references.
Dr. Triboulet educating around glial cells! --- Support this podcast: https://anchor.fm/ashley-triboulet/support
Introduction to the podcast and topics that will be discussed. --- Support this podcast: https://anchor.fm/ashley-triboulet/support
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